<div><strong>Background:</strong> miR-140-5p is frequently dysregulated in different types of tumors and has been found to suppress inflammation through TLR4 in lung injury. In the current investigation, we try to decipher the possible function of miR-140-5p in hypoxia-induced nephrotoxicity and renal fibrogenesis in human renal cells.&nbsp;<br />
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<strong>Methods:</strong> Hypoxia in HK-2 cells was produced using cobalt chloride (CoCl2). Hypoxia-induced cellular viability and apoptosis were determined by cell viability assay and ELISA-based apoptosis assay, respectively. Western blotting was carried out to measure expression levels of pro-fibrotic and apoptosis-related proteins.&nbsp;<br />
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<strong>Result: </strong>The present study observed that upregulation of miR-140-5p significantly decreases apoptosis and increases cell viability in hypoxia challenged HK-2 cells. Furthermore, miR-140-5p over expression decreased expression of pro-apoptotic proteins like Bad and Bax and pro-fibrotic proteins like Collagen I, CTGF and fibronectin. While as, expression of anti-apoptotic protein, namely Bcl-2, was increased in hypoxia-insulted HK-2 cells. Moreover, the luciferase reporter assay confirmed that miR-140-5p targets TLR4. TLR4 knockdown prevents miR-140-5p from performing its suppressive role in hypoxia linked to apoptosis and fibrosis.&nbsp;</div>


<p>MicroRNA-140-5p Suppresses Hypoxia-induced Nephrotoxicity and Renal Fibrogenesis in <em>in vitro</em> Conditions</p>


<div style="text-align: justify;">Fibrosis is a common finding in chronic mastitis. Epithelial-mesenchymal transition (EMT) plays a prominent role in fibrogenesis in adult tissues. The aim of this study was to investigate whether EMT occurs in bovine mastitis by assessing the expression or localization of alpha-smooth muscle actin (alpha-SMA), S-100 protein and caspase-3. Two normal bovine mammary gland tissue samples and five mastitic samples were used in the study. Antibodies to alpha-SMA, S-100 and caspase-3 were used for immunohistochemical studies. In mastitis there was increased expression of S-100 in the alveolar epithelial cells. Alpha-SMA was highly expressed in the areas where there is fibrosis in chronic mastitis. Further caspase-3 was observed in alveolar cells in mastitic tissue. Overexpression of S-100 and alpha-SMA directly correlates to the severity of mastitis.S-100 and alpha-SMA may serve as biomarkers to know the extent of tissue structural changes in mastitis. EMT could be one of the mechanistic pathways underlying the pathogenesis of fibrosis in mastitis.&nbsp;</div>

MicroRNA-140-5p Suppresses Hypoxia-induced Nephrotoxicity and Renal Fibrogenesis in in vitro Conditions

Immunohistochemical detection of alpha-smooth muscle actin and S-100 in bovine mammary gland with mastitis